The focus of the proposed work is upon understanding the neural and behavioral mechanisms which underlie the dramatic recovery of visually guided behavior in the cat that has been termed the "Sprague effect". In a motivated animal when a stimulus enters into a part of the visual field the animal responds with a coordinated movement of the head, eyes, pinnae, and body towards the stimulus. This "orienting response" is permanently lost in the visual hemifield contraclateral to a large unilateral visual cortical lesion. In such an hemianopic animal however if the superior colliculus (SC) opposite to the cortical lesion is ablated or if the commissure between the two SC is cut, the orienting response rapidly recovers in the previously blind hemifield. Sprague hypothesized that the two SC normally inhibit each other and that the recovery seen in the Sprague effect (SE) is due to the release of the colliculus ipsilateral to the cortical lesion from the tonic inhibition exerted by its counterpart on the other side. Recent experiments from our laboratory show that this hypothesis is inadequate to explain the SE and that other subcortical nuclei, pathways, and mechanisms are likely responsible. The goal of the proposed studies is to learn what they are. We propose: 1) to determine what portion of the commissure of the superior colliculus (CSC) must be cut to produce the SE; 2) to determine whether ibiotenic acid injections into the SC opposite a visual cortical lesion result in the SE and to assess the effects of such lesions in normal cats; 3) to determine what fiber pathways course through the CSC, using both orthograde and retrograde labelling methods; and 4) to determine the efficacy of each of the above identified subcortical nuclei in producing the SE. Understanding the neural mechanisms that mediate this recovery of visual function may have direct implications for therapeutic interventions in humans suffering from syndromes of sensory loss or neglect.